Endocrine Abstracts (2017) 49 EP870 | DOI: 10.1530/endoabs.49.EP870

Central diabetes insipidus and cerebral salt wasting syndrome: a challenging coexistence

Maria Manuel Costa1,2, Cesar Esteves1,3, José Luis Castedo1, Josué Pereira2,4 & Davide Carvalho1,3

1Department of Endocrinology, Diabetes and Metabolism of Centro Hospitalar de São João, Porto, Portugal; 2Faculty of Medicine, University of Porto, Porto, Portugal; 3Instituto de Investigação e Inovação da Saúde da Universidade do Porto, Porto, Portugal; 4Department of Neurosurgery of Centro Hospitalar de São João, Porto, Portugal.

Introduction: Combined central diabetes insipidus (DI) and cerebral salt wasting syndrome (CSW) is a rare clinical finding. However, when this happens, mortality is high due to delayed diagnosis and/or inadequate treatment.

Case report: 42-year-old man referred to neurosurgery due to a non functional pituitary macroadenoma with bitemporal hemianopsia. He underwent partial ressection of the tumour on July 2nd 2015. On the following day of surgery he presented poliuria with sodium (Na) 149 mEq/l, plasma osmolality (pOsm) 301 mOsm/kg and urine osmolality (uOsm) 293 mOsm/kg. He started nasal desmopressin 0.05 mg/day with good response. He was already on dexamethasone 4mg and levothyroxine 75 μg due to hypopituitarism. On july 9th he became confused. Cerebral CT was performed with no significant changes. His natremia dropped to 128 mEq/l, with development of poliuria despite maintenance of desmopressin doses. Hemoglobin and hematocrit rose from 9.1 g/l to 11.6 g/l and 27.5–32.5, respectively. Thyroid function was normal and the patient was on hydrocortisone 30 mg/day. At 1200 h he initiated 150 mg/hydrocortisone infusion, but Na did not increased. Plasma and urine osmolality were 264 mOsm/kg and 679 mOsm/kg, respectively. At 1600 h hydrocortisone was increased and hypertonic saline replacements started. At 1800 h he was dehydrated with poliuria and vomiting and natremia of 124 mEq/l. Hyponatraemia was very resistant to treatment despite hypertonic saline replacements, hence desmopressin was suspended. On next day urine spot analysis showed that natriuresis was 63 mEq/l with serum sodium 132 mEq/l. This was interpreted as CSW and control was achieved with aggressive hypertonic saline replacements and fludrocortisone 0.1 mg/tid. Two days after, Na levels were normalized and desmopressin was restarted. Hypertonic saline dose was gradually decreased and switched to sodium chloride tablets. He was discharged on fludrocortisone 0.1 mg/bid, oral sodium chloride 16 g/day, oral desmopressin 0.1 mg/bid, hydrocortisone 20 mg/day, levothyroxine 100 μg/id. Two months later he was only on hydrocortisone, desmopressin and levothyroxine.

Conclusion: We presented a rare case of a patient with DI and CSWS successfully treated. Hyponatremia in a DI patient may erroneously be interpreted as inadequate DI control leading to therapeutic errors. Thus, all clinical and analytical data should be evaluated together for an early and proper diagnosis.

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